|1.||Pulido, Rafael: 2 articles (07/2014 - 11/2006)|
|2.||Devreotes, Peter: 2 articles (07/2014 - 04/2005)|
|3.||Ross, Alonzo H: 2 articles (07/2014 - 07/2004)|
|4.||Burgess, Antony W: 2 articles (11/2010 - 07/2009)|
|5.||Catimel, Bruno: 2 articles (11/2010 - 07/2009)|
|6.||Condron, Melanie: 2 articles (11/2010 - 07/2009)|
|7.||Holmes, Andrew B: 2 articles (11/2010 - 07/2009)|
|8.||Ooms, L M: 1 article (07/2015)|
|9.||Tan, A: 1 article (07/2015)|
|10.||Bukczynska, P E: 1 article (07/2015)|
09/01/2014 - "PTEN, a tumor suppressor that is frequently mutated in a wide spectrum of cancers, exerts PI(3,4,5)P3 phosphatase activities that are regulated by its dynamic shuttling between the membrane and cytoplasm. "
09/01/2013 - "DHA also inhibits AKT(T308) but not AKT(S473) phosphorylation, alters PI(3,4,5)P3 (PIP3) and phospho-AKT(S473) protein localization, decreases pPDPK1(S241)-AKT and AKT-BAD interaction and suppresses prostate tumor growth. "
01/01/2013 - "Cancer cells resistant to therapy promote cell surface relocalization of GRP78 which complexes with PI3K and enhances PI(3,4,5)P3 production."
01/01/2015 - "The role of phosphatase and tensin homolog on chromosome 10 (PTEN) as a tumor suppressor has been for a long time attributed to its lipid phosphatase activity against PI(3,4,5)P3, the phospholipid product of the class I PI3Ks. "
09/15/2014 - "Production of the phosphoinositide lipid phosphatidylinositol (3,4,5)trisphosphate [PI(3,4,5)P3, or PIP3] by class I phosphoinositide 3-kinases (PI3Ks) is a major signaling mechanism whose deregulation contributes to serious diseases, including cancer. "
|2.||Glioblastoma (Glioblastoma Multiforme)
07/01/2015 - "The tumor suppressor gene PTEN is deleted, mutated or hypermethylated in more than 60% of glioblastoma cases resulting in hyperactivation of the phosphoinositide 3-kinase pathway, which leads to sustained PI(3,4,5)P3 signaling, and thereby hyperactivation of Akt and other effectors. "
01/01/2014 - "In the glioblastoma cell line 1321 N1, that do not express PTEN, lowering SHIP2 expression has an impact on the levels of PI(3,4,5)P3, cell morphology and cell proliferation. "
07/01/2015 - "PI(3,4,5)P3 is also hydrolyzed to PI(3,4)P2 by inositol polyphosphate 5-phosphatases such as SKIP, but the role this pathway has in glioblastoma is unknown. "
10/22/1998 - "We show that glioblastoma cells, in contrast to primary human astrocytes, contain high endogenous protein kinase B (PKB/Akt) activity and high levels of PI 3,4,5-triphosphate (PI(3,4,5)P3) and PI(3,4)P2, the lipid products of PI 3-kinase. "
02/01/2005 - "SHIP2 is a physiologically important negative regulator of insulin signalling hydrolysing the PI3-kinase product, PI(3,4,5)P3, which also has an impact on insulin resistance. "
05/01/2005 - "Src homology 2-containing 5'-inositol phosphatase 2 (SHIP2) is known to be one of lipid phosphatases converting PI(3,4,5)P3 to PI(3,4)P2 in the negative regulation of insulin signaling with the fundamental impact on the state of insulin resistance. "
10/01/2014 - "Expression of PI4KIIIβ in breast carcinoma cells leads to increased Akt activation, dependent on increased PI(3,4,5)P3 production. "
11/01/2010 - "This methodology allows the analysis of PI(3,4,5)P3 subcellular distribution in resting and epidermal growth factor (EGF)-stimulated HEK293T cells and in LIM1215 (wild-type phosphoinositide 3-kinase (PI3K)) and LIM2550 (H1047R mutation in PI3K catalytic domain) colonic carcinoma cells. "
|5.||Thymoma (Thymic Carcinoma)
|5.||Proto-Oncogene Proteins c-akt (Protein Kinase B)
|8.||Phosphatidylinositol 3-Kinase (1 Phosphatidylinositol 3 Kinase)
|10.||PTEN Phosphohydrolase (PTEN Phosphatase)
|1.||Drug Therapy (Chemotherapy)